"Now that we understand how the virus operates, we can develop vaccines and drugs to block Nipah from entering the cells. This will help prevent infection and halt outbreaks before they reach epidemic proportions,” said Dr. Benhur Lee, principal investigator and UCLA assistant professor of microbiology, immunology and molecular genetics.

Since 1998, the Nipah virus has triggered disease outbreaks in Australia, Singapore, Malaysia and Bangladesh. Animals spread the virus to people, where it causes life-threatening respiratory and neurological diseases that kill up to 70 percent of patients - a danger level equivalent to the Ebola virus.

To infect a cell, viruses must bind to a viral-specific receptor on the cell's surface in order to penetrate it. Lee's team identified a cell receptor called Ephrin-B2 as the key used by the Nipah virus to unlock the cells.

Located on brain cells and cells lining the blood vessels, Ephrin-B2 is critical to nervous system development and the growth of blood vessels in human and animal embryos. Ephrin-B2 is found in humans, horses, pigs and bats, which may explain why the infection can jump so easily from one species to another.

To confirm their findings, the UCLA team engineered a harmless virus with Nipah virus proteins embedded in its coat. The decoy virus successfully infected cells vulnerable to the Nipah virus, but could not infect Nipah-resistant cells.

In the final step, the decoy virus entered nerve cells and cells lining blood vessels by latching onto Ephrin-B2, proving that the receptor is the same doorway that the real Nipah virus enters to infect these cells. "We now can screen for small molecules that will block viral entry via Ephrin B-2 and develop them as therapeutic drugs,” said Lee.